Post Polio is a condition that affects up to 8% of persons who survive paralytic polio; can develop as late as, 30, 40 years after the initial recovery; symptoms vary from mild weakness to severe fatigue and disability .
Fibromyalgia and diabetic neuropathy have a couple of things in common. Both conditions involve seemingly unexplainable pain, tingling, and can drastically reduce your quality of life.
Early research suggests that cannabis may have powerful therapeutic effects for both conditions, and this new pain patch offers a novel new approach for conditions that are incredibly difficult to treat.
A 2014 survey from the National Pain Foundations found that cannabis was considered the most effective pain medication by fibromyalgia patients who were willing to experiment with the herb.
Not all survey respondents had consumed cannabis. However, those that had suggested that the herb worked better at managing pain than the leading prescriptions for fibromyalgia, including Savella, Cymbalta, and Lyrica.
Small human trials of cannabis for diabetic neuropathy have also been successful. A study of 16 patients with diabetic neuropathy of the feet found the herb successfully reduced pain symptoms in a dose-dependant manner. The cannabis plant has successfully reduced nerve pain associated with conditions like multiple sclerosis as well.
While expensive cannabis-based pharmaceuticals are already available in some countries for the treatment of nervous disorders, most canna-curious patients are stuck with topical creams and oral cannabis options, which can be a little strong for the daytime.
Now, one innovative company, Cannabis Science, has released a revolutionary new topical application of cannabis medicines.
Cannabis Science designs an infused pain patch
Cannabis Science, Inc. is a pharmaceutical research company that works to develop innovative new cannabis medicines. In November of 2016, they announced their most recent project, a transdermal patch that delivers powerful pain-fighting medicine through the skin and into the bloodstream.
The company has two new patches in mind, one for fibromyalgia and one for diabetic neuropathy. While both of these patches will contain cannabinoids, each formulation and delivery method will be designed to most effectively manage symptoms of the respective illness.
In a press release announcing the new pain patch, Cannabis Science CEO Raymond Dabney explains,
The development of these two new pharmaceutical medicinal applications are just the tip of the iceberg for what we see as the future for Cannabis Science.
While we strive to increase our land capacity for growth and facilities to produce our own product to supply our scientists with proprietary materials to make these formulations, we are also busy researching more potential needs for Cannabis related medical applications and developing the methods for delivery of these medications.
Earlier in 2016, Cannabis Science began recruiting for a study on inhaled cannabis preparations for patients with asthma and lung diseases like COPD.
Cannabis Science is also not the first company to look into the transdermal applications of cannabis. Mary’s Medicinals got there first, offering cannabis-infused pain patches to medical cannabis patients in Colorado, Arizona, Nevada, Washington, Michigan, and Oregon. The company also hopes to offer their patches in California soon.
Excerpts from The Polio Paradox, 2002, by Richard L. Bruno who estimated 1.63 million polio survivors in the US. [p6] “There were more polio survivors than those with Parkinson’s disease, multiple sclerosis and spinal cord injury combined”…”the cause and treatment of PPS involved both body and mind”, or Dr. Bruno’s specialty: physicopsychology, for which he holds a PhD.
[p12] “There are clear parallels dating from as far back as 1935 between polio and what in the 1980s came to be called Chronic Fatigue Syndrome”…”Twenty million more individuals with a variety of disabilities..are also experiencing fatigue, muscle weakness, and pain in mid-life, and seeing their abilities ebb away”
[p15] “In 1875 an unusual case was presented to the Society of Biology in Paris. A nineteen-year-old patient had had polio when he was six months old that paralyzed his left side…The young man had recovered partial use of his left arm and leg and became a tanner, which required him to use his arms to pull heavy, wet hides out of vats of acid. By the time he was seventeen, this French patient reported fatigue and a feeling of heaviness in his right arm, the arm that had apparently not been affected by the polio. His right arm and leg both became weaker and smaller”…
On hearing this presentation, the renowned French neurologist Jean-Martin Charcot concluded that the young tanner’s new weakness was due to overusing his stronger right arm, damage done by the poliovirus somehow having ‘moved’ from the left side of his body to the right.
That same year, three other French doctors described other polio survivors who had developed muscle weakness and atrophy, a shrinking of the muscles, fifteen to almost thirty years after they had polio. From 1875 to 1900, twenty-four articles appeared in European medical journals describing 30 additional polio survivors experiencing new weakness and sometimes atrophy..in limbs that obviously had been affected during the polio attack, but also in limbs that had..been unaffected. In 1899 British doctor William Hirsch reviewed all the cases reported during the nineteenth century. He concluded that there were three possible causes for late-onset weakness in polio survivors: (1) The poliovirus had damaged spinal cord motor neurons –the cells that make muscles contract– making them vulnerable to some other disease later in life; (2) Certain individuals were susceptible to developing motor neuron diseases..that allowed them to get polio as children and then develop another disease called ‘progressive muscular atrophy’ later in life; (3) Spinal cord motor neurons had been ‘scarred’ by the poliovirus, setting the stage for a ‘flare-up’ at a later date which caused new weakness.
[p16] Hirsch was the first to suggest that the poliovirus could somehow damage neurons early in life, damage that..caused new muscle weakness many years later.
In 1903 Charles Potts wrote the twentieth century’s first article on the late effects of polio –the first to appear in an American medical journal in which he too reviewed the nineteenth-century cases. Potts concluded that two of the polio survivors described had ALS –amyotrophic lateral sclerosis..(Lou Gehrig’s disease)– a fatal disease that causes progressive paralysis of muscles throughout the the body as a result of the death of the spinal cord motor neurons. However, Potts added that the overwhelming majority of the polio survivors described thus far..did not have ALS but instead had progressive muscular atrophy [as] Hirsch had mentioned, a disease of unknown origin…
In 1936, New York neurologists Salmon and Riley..supposed..the new and frightening notion that the poliovirus might lie dormant in the spinal cord and somehow cause muscle weakness decades later…
[p17] The dearth of articles between 1936 and 1960 about the late effects in polio survivors is undoubtedly due to polio’s incidence reaching epidemic proportions. All of medicine was focused on dealing with the acute problems being experienced by the hundreds of thousands of individuals infected with the poliovirus during those years, and on developing a polio vaccine. But articles about late-onset problems appeared again. A 1962 British paper by K.J. Zilkha was the first to follow the course of muscle weakness in polio survivors over many years…
In 1970, three British lung specialists reported…polio patients who were experiencing not only muscle weakness but also “excessive fatigue”, “breathlessness”, an inability to concentrate, drowsiness, and “severe attacks of sleepiness”. These patients also reported “abnormal sensitivity to cold, especially of the extremities”…
[p18] And in 1980 a group of Italian doctors…concluded that although only one hundred cases had been described in the preceeding 105 years, late-onset problems in polio survivors were “far from rare”. They agreed..that late-onset symptoms represented a “new process distinguishable from the old disease”.
Chapter Three “The Guided Missile”…
[p20].. quoting researcher David Bodian: “The average number of spinal cord motor neurons that are destroyed by the poliovirus is almost 50%. However, nonparalytic polio may be associated with severe neuron damage in the spinal cord. What is more, some with nonparalytic poliomyelitis do not have any damage in the spinal cord but have charateristic damage in the brain, which is more extensive than in some who did have paralysis. All available evidence shows conclusively that every case of polio exhibits damage in the brain. The poliovirus is capable of producing an encephalitis, with or without symptoms, in the absence of any damage to the spinal cord. As far as the pathologist is concerned all cases of polio are encephalitic”.
[p21] It’s amazing that something so small can do so much damage…But the poliovirus doesn’t attach to and damage just any cell. It is a ‘guided missile’ that does one thing: seek out, damage, and destroy the neurons that “activate” you –the ones that activate your brain and muscles. The poliovirus is the perfect human “Off switch”…
[p23] The existence of dozens of poliovirus strains makes it clear that polioviruses mutate inside people and can change their virulence. In fact, experiments in animals show that the passage of poliovirus –infecting one animal with a poliovirus, having that animal infect another, and so on– can increase virulence. As polioviruses passed from person to person during the middle of the twentieth century, they apparently became more virulent, causing more paralysis and killing more people in 1950 than they did in 1920…
[p24]…Poliovirus released from both your tonsils and intestines also traveled to the large lymph nodes under your arms…finally, about ten days after you were infected..huge amounts of virus spilled into your bloodstream..[carrying] its deadly cargo toward its intended destination : the neurons in your brain and spinal cord.
[p25] Virus-laden blood flowed up into your head and found “leaky” places in the brain’s blood vessels, where poliovirus flowed into the brain. At the same time, infected monocytes passed throught the walls of brain blood vessels acting like ‘poliovirus taxis’ that also allowed virus to enter the brain…
[p26] Once inside those neurons..[they] travelled inside neurons to penetrate more deeply…Then the poliovirus could head south, descending inside spinal cord neurons and ending up in the motor neurons…
There’s yet a third way poliovirus could reach brain and spinal cord motor neurons…such as [flowing] out of the Peyer’s patches and enter the vagus nerve –the nerve that makes the intestines contract– inside which they can travel all the way up to the brain…What’s more, motor neurons are covered with poliovirus receptors where they make contact with your muscles. When your blood was full of virus, damaging a muscle and puncturing a blood vessel could bathe neurons with virus…children whose muscles had been slightly daamaged by an injection were up to ten times more likely to get paralytic polio –and were most often paralyzed in the limb where they received the injection.
After a poliovirus latches on..to the surface of a neuron [it] causes it to ‘unzip’, releasing its contents inside the neuron. [These are] about a dozen individual proteins..that shut down and then literally break apart the ‘factories’ that manufacture [what] a neuron needs…
[p27]..the neuron can no longer make neurochemicals –the proteins that allow one neuron to talk to another and that allow motor neurons to make muscles contract. When neurochemicals stop being made, the neuron’s ‘OFF’ switch id thrown.
[p29] The poliovirus is remarkable in its ability to invade neurons. In the 1940s..Bodian found that 96% of motor neurons were infected by the poliovirus if you had any paralysis at all!
But..on average, 50% of all motor neurons are destroyed…Bodian discovered that at least 60%..must be killed before [a] muscle shows any weakness at all.
[p30] Unfortunately, there’s even more to the aftermath of polio than losing about half of your motor neurons…those recovered neurons were never the same as they were before the poliovirus invaded. Damaged and rebuilt neurons are smaller and also have shrunken axons –the cable-like extensions that travel out..to connect with muscles.
[p31] What’s more, the microscopic tubules within the neurons were ‘plugged’ with debris that was probably created when the poliovirus broke apart the neuron…like clogged pipes, plugged tubules can’t carry all the proteins, nutrients, and neurochemicals where they need to go…
[p33] In Latin,[Greekactually] polio means ‘gray’…gray neurons are those not covered in myelin, the white fatty insulation that separates one neuron from another….
[p34]..In fact, the main event of the poliovirus attack was not in the spinal cord at all. [more excerpts on The Polio Paradox page]